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Presynaptic Deletion of GIT Proteins Results in Increased Synaptic Strength at a Mammalian Central Synapse.
- Source :
-
Neuron [Neuron] 2015 Dec 02; Vol. 88 (5), pp. 918-925. - Publication Year :
- 2015
-
Abstract
- A cytomatrix of proteins at the presynaptic active zone (CAZ) controls the strength and speed of neurotransmitter release at synapses in response to action potentials. However, the functional role of many CAZ proteins and their respective isoforms remains unresolved. Here, we demonstrate that presynaptic deletion of the two G protein-coupled receptor kinase-interacting proteins (GITs), GIT1 and GIT2, at the mouse calyx of Held leads to a large increase in AP-evoked release with no change in the readily releasable pool size. Selective presynaptic GIT1 ablation identified a GIT1-specific role in regulating release probability that was largely responsible for increased synaptic strength. Increased synaptic strength was not due to changes in voltage-gated calcium channel currents or activation kinetics. Quantitative electron microscopy revealed unaltered ultrastructural parameters. Thus, our data uncover distinct roles for GIT1 and GIT2 in regulating neurotransmitter release strength, with GIT1 as a specific regulator of presynaptic release probability.<br /> (Copyright © 2015 Elsevier Inc. All rights reserved.)
- Subjects :
- Animals
Animals, Newborn
Biophysics
Cell Cycle Proteins genetics
Electric Stimulation
GTPase-Activating Proteins genetics
Green Fluorescent Proteins genetics
Green Fluorescent Proteins metabolism
In Vitro Techniques
Intercellular Signaling Peptides and Proteins
Mice
Mice, Knockout
Microscopy, Electron, Transmission
Patch-Clamp Techniques
Phosphoproteins deficiency
Phosphoproteins genetics
Probability
Synapses metabolism
Synapses ultrastructure
Transduction, Genetic
Vesicular Glutamate Transport Protein 2 metabolism
Brain cytology
Cell Cycle Proteins deficiency
Excitatory Postsynaptic Potentials genetics
GTPase-Activating Proteins deficiency
Synapses genetics
Subjects
Details
- Language :
- English
- ISSN :
- 1097-4199
- Volume :
- 88
- Issue :
- 5
- Database :
- MEDLINE
- Journal :
- Neuron
- Publication Type :
- Academic Journal
- Accession number :
- 26637799
- Full Text :
- https://doi.org/10.1016/j.neuron.2015.10.042